REPORT Was a ÔhyperdiseaseÕ responsible for the late Pleistocene megafaunal extinction? S. Kathleen Lyons, 1 * Felisa A. Smith, 1 Peter J. Wagner, 2 Ethan P. White 1 and James H. Brown 1 1 Department of Biology, University of New Mexico, Albuquerque, NM 87131, USA 2 Department of Geology, Field Museum of Natural History, Chicago, IL 60605, USA Present address: S. Kathleen Lyons, National Center for Ecological Analysis and Synthesis, University of California – Santa Barbara, Santa Barbara, CA 93101, USA. *Correspondence: E-mail: lyons@nceas.ucsb.edu Abstract Numerous hypotheses have been proposed to explain the end Pleistocene extinction of large bodied mammals. The disease hypothesis attributes the extinction to the arrival of a novel ÔhyperdiseaseÕ brought by immigrating aboriginal humans. However, until West Nile virus (WNV) invaded the United States, no known disease met the criteria of a hyperdisease. We evaluate the disease hypothesis using WNV in the United States as a model system. We show that WNV is size-biased in its infection of North America birds, but is unlikely to result in an extinction similar to that of the end Pleistocene. WNV infects birds more uniformly across the body size spectrum than extinctions did across mammals and is not size-biased within orders. Our study explores the potential impact of WNV on bird populations and provides no support for disease as a causal mechanism for the end Pleistocene megafaunal extinction. Keywords Disease hypothesis, end-Pleistocene extinctions, mammals, megafauna, size-biased extinctions, West Nile virus. Ecology Letters (2004) 7: 859–868 INTRODUCTION The mammalian faunas of Australia and the New World are depauperate today. Before the arrival of humans, each continent contained an assemblage of large-bodied mam- mals that rivaled that of modern Africa. The New World contained numerous species of mastodons, ground sloths, camels, and horses; marsupials the size of rhinoceros inhabited Australia (Smith et al. 2003). Approximately, 12 000 years ago in the New World (Fiedel 1999; Thorne et al. 1999) and 46,000 years ago in Australia (Roberts et al. 2001), the largest species in each fauna went extinct (Martin & Klein 1984; MacPhee 1999; Lyons et al. 2004). The ultimate causes of this extinction fall into three general categories: (1) environmental change, which attributes the extinction of the megafauna to changes in climate and vegetation (Guilday 1967; Graham & Lundelius 1984), (2) human predation, which attributes the extinction to hunting by newly arrived aboriginal humans (Martin 1967, 1984), and (3) disease, which attributes the extinction to diseases brought by newly arrived aboriginal humans (MacPhee & Marx 1997). The first two hypotheses have been exhaus- tively debated in the literature (e.g. Martin & Klein 1984; MacPhee 1999 and references therein). Here, we focus on the disease hypothesis. The disease hypothesis attributes the extinction of large mammals during the late Pleistocene to indirect effects of the newly arrived aboriginal humans (MacPhee & Marx 1997). It proposes that humans or their commensals introduced one or more highly virulent diseases into vulnerable populations of native mammals, eventually causing extinctions. The failure of several prior immigra- tions of mammals into North America from Eurasia throughout the Cenozoic to yield widespread extinction necessarily implicates humans or their commensals as the disease vector. Small-bodied species are postulated to have a greater population resilience due to their life history traits (e.g. shorter gestation time, greater population sizes, etc.), causing the extinction event to be biased toward larger-sized species (MacPhee & Marx 1997). If a disease was indeed responsible for the end- Pleistocene extinctions, then there are several criteria it must satisfy (see Table 7.3 in MacPhee & Marx 1997). First, the pathogen must have a stable carrier state in a reservoir species. That is, it must be able to sustain itself in the environment when there are no susceptible hosts available to infect. Second, the pathogen must have a high infection rate, such that it is able to infect virtually all individuals of all ages and sexes encountered. Third, it must be extremely lethal, with a mortality rate of c. 50–75%. Finally, it must Ecology Letters, (2004) 7: 859–868 doi: 10.1111/j.1461-0248.2004.00643.x Ó2004 Blackwell Publishing Ltd/CNRS